In a patient presenting with chest pain suggestive of acute coronary syndrome, an ECG showing left ventricular hypertrophy with strain pattern in leads V5‑V6, and a high‑sensitivity cardiac troponin T of 24 ng/L, what is the most likely diagnosis?

Most Likely Diagnosis: Non-ST-Elevation Myocardial Infarction (NSTEMI)

In a patient presenting with chest pain suggestive of acute coronary syndrome, an ECG showing left ventricular hypertrophy with strain pattern in V5-V6, and a high-sensitivity cardiac troponin T of 24 ng/L, the most likely diagnosis is NSTEMI, though the LVH with strain pattern significantly complicates ECG interpretation and may mask or mimic ischemic changes. 1

Diagnostic Reasoning

Troponin Interpretation

• A hs-cTnT of 24 ng/L is elevated above the 99th percentile (typically 14 ng/L for most assays), indicating myocardial injury 1
• Serial troponin measurements at 3-6 hour intervals are mandatory to establish a rising/falling pattern (≥20% change) that confirms acute myocardial necrosis rather than chronic elevation 1, 2
• Approximately 10-15% of patients with true myocardial injury may have normal initial troponin, making repeat testing essential 1, 2
• The absolute level of 24 ng/L is modest; troponin concentrations >5× the upper reference limit (>70 ng/L) have >90% positive predictive value for acute type 1 MI 1, 3

ECG Challenges with LVH

• The diagnostic challenge arises because LVH with strain pattern itself produces ST-segment depression and T-wave abnormalities in lateral leads (V5-V6) that can mimic or mask acute ischemia 1, 4
• LVH causes secondary repolarization abnormalities with ST-segment changes independent of coronary disease 4, 5
• Approximately 63% of patients with LVH show the typical "strain pattern" (ST depression with asymmetrical T-wave inversion), while 37% show non-specific ST-T changes that cannot be distinguished from coronary disease 5
• Comparison with a previous ECG is critical—new or dynamic ST-segment changes superimposed on baseline LVH would strongly suggest acute ischemia 1, 4

Clinical Context Integration

• The presence of chest pain consistent with ACS combined with elevated troponin meets criteria for NSTEMI, regardless of ECG ambiguity 1
• LVH itself can cause subendocardial ischemia through altered coronary blood flow and increased oxygen demand, potentially leading to type 2 MI (supply-demand mismatch) 6
• Patients with electrocardiographic LVH and NSTEMI have a 32% prevalence of non-obstructive coronary disease (<50% stenosis), compared to 22% in those without LVH 6

Immediate Diagnostic Steps

Serial Troponin Testing

• Obtain repeat hs-cTnT at 3-6 hours after the initial measurement 1, 2
• A ≥20% rise or fall with at least one value above the 99th percentile confirms acute myocardial necrosis 1
• If using 0/1h or 0/2h accelerated protocols, apply assay-specific cutpoints and delta values 3

ECG Monitoring

• Obtain serial 12-lead ECGs every 15-30 minutes during the first hour if symptoms persist 1, 2
• Look for dynamic changes: new ST-segment depression ≥1 mm beyond baseline LVH pattern, transient ST-elevation, or evolving T-wave inversions 1
• Consider posterior leads (V7-V9) and right-sided leads (V3R-V4R) to detect ischemia in territories not well-represented by standard leads 1, 4

Clinical Assessment

• Document chest pain characteristics: duration >20 minutes, radiation to left arm/jaw/neck, associated diaphoresis, nausea, or dyspnea 1
• Assess for hemodynamic instability, signs of heart failure (pulmonary edema, elevated JVP), or new cardiac murmurs 1
• Identify precipitating factors: anemia, infection, tachyarrhythmias, severe hypertension that could cause type 2 MI 1

Differential Diagnosis

Type 1 MI (Thrombotic ACS)

• Most likely if troponin shows rising pattern, ischemic symptoms persist >20 minutes, and dynamic ECG changes emerge 1
• Risk factors: known CAD, diabetes, hypertension, hyperlipidemia increase likelihood 1

Type 2 MI (Supply-Demand Mismatch)

• LVH itself increases myocardial oxygen demand and can cause subendocardial ischemia without plaque rupture 3, 6
• Consider if tachycardia (HR >120 bpm), severe hypertension (>180/110 mmHg), anemia, or hypotension present 1, 3

Non-Ischemic Causes of Troponin Elevation

• Acute decompensated heart failure: LVH predisposes to diastolic dysfunction; look for pulmonary edema, elevated BNP 1, 3
• Myocarditis: may present with chest pain and troponin elevation; consider if viral prodrome or inflammatory markers elevated 1, 3
• Takotsubo cardiomyopathy: can mimic ACS with ST-changes and troponin rise; more common in postmenopausal women with emotional stress 3, 4
• Chronic kidney disease: check creatinine; eGFR <30 mL/min causes persistently elevated troponin 1, 3

Management Algorithm

If Rising/Falling Troponin Pattern Confirmed (NSTEMI)

1. Initiate dual antiplatelet therapy immediately: aspirin 162-325 mg loading dose plus P2Y12 inhibitor (ticagrelor or prasugrel preferred) 1, 2
2. Start anticoagulation: unfractionated heparin, low-molecular-weight heparin (enoxaparin), or bivalirudin 1, 2
3. Calculate GRACE risk score: if >140, perform urgent coronary angiography within 24 hours 1, 2
4. Consider GP IIb/IIIa inhibitor (eptifibatide or tirofiban) in high-risk patients proceeding to angiography 1, 2
5. Continuous cardiac monitoring for at least 24 hours given arrhythmia risk 2

If Stable/Flat Troponin (Chronic Elevation)

1. Perform bedside echocardiography to assess LV function, wall motion abnormalities, LV wall thickness, and exclude alternative diagnoses 1, 3
2. Treat underlying condition: optimize blood pressure control if hypertensive heart disease, manage heart failure if present 3
3. Outpatient cardiology follow-up for risk stratification and consideration of stress testing or coronary CT angiography 3

Critical Pitfalls to Avoid

• Never dismiss troponin elevation as "false-positive" due to LVH—it represents genuine myocardial injury with prognostic significance 3
• Never rely on a single troponin measurement—serial testing is mandatory to distinguish acute from chronic injury 1, 2
• Never attribute troponin elevation solely to LVH or renal dysfunction without evaluating for concurrent acute coronary disease 3
• Do not use point-of-care troponin assays for serial monitoring—they have substantially lower sensitivity than central laboratory high-sensitivity methods 1, 3
• Recognize that patients with LVH and chest pain represent the highest-risk group for adverse outcomes, even higher than those with primary ST-deviation, requiring aggressive evaluation despite ECG ambiguity 4

Prognostic Implications

• Any troponin elevation confers approximately 3-fold increased risk of death or MI at 30 days, independent of underlying cause 1, 3
• The magnitude of troponin elevation correlates directly with mortality risk 1, 3
• Patients with electrocardiographic LVH and NSTEMI have lower rates of in-hospital revascularization (45% vs 69%) but similar outcomes when appropriately managed 6